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Hospital Practitioner Department of Hepatology and Gastroenterology Begin Military Hospital 69 avenue de Paris 94160 Saint-Mandé, France fax 33 (0)1 43 98 53 63 mennecier{at}hepatoweb.com
Hospital Practitioner Department of Biochemistry Begin Military Hospital
Hospital Practitioner Department of Biochemistry Begin Military Hospital
Hospital Practitioner Department of Hepatology and Gastroenterology Begin Military Hospital
Published Online, March 1, 2005. www.theannals.com, DOI 10.1345/aph.1E292
Case Report. On August 15, 2002, an 81-year-old white woman was hospitalized with unusual lethargy. Her past medical history revealed concentric cardiomyopathy secondary to hypertension, stabilized for the past 2 years by spironolactone 75 mg daily, and a recurring gastroesophageal reflux requiring maintenance therapy with lansoprazole for the past 3 years. Routine blood testing had shown normal sodium levels of 134 mEq/L one month before her admission. On August 10, 2002, lansoprazole was replaced by esomeprazole 20 mg daily. Subsequently, the woman started to complain of asthenia and consciousness disturbance, requiring her to be hospitalized.
Physical examination on admission showed BP 130/65 mm Hg without orthostatic hypotension, HR 70 beats/min with regular rhythm, and T 36.9 °C. There were no abnormal findings in the chest, abdomen, or extremities. There were no signs of dehydration or edema. The neurologic examination confirmed a consciousness disturbance without any other neurologic disorder. Blood chemistry showed hyponatremia (sodium 122 mEq/L). Other blood chemistry parameters were within normal ranges. There were no abnormal findings in brain computed tomography scan, chest X-ray, and electrocardiogram. Plasma and urinary osmolality were 275 mOsm/kgH2O (reference range 280–310) and 351 mOsm/L (reference range 50–1400), respectively, with natriuresis of 80 mmol/24h. Plasma antidiuretic hormone (ADH) was 1.8 mmol/L (reference range <7.4) and hepatic, thyroid, and adrenal chemistry values were normal.
As drug-related hyponatremia was suspected, esomeprazole was discontinued on the day of admission and the woman was placed under fluid restriction of 1000 mL/day while continuing spironolactone therapy. Psychomotor dysfunction disappeared within 48 hours as normalization of the blood sodium level and plasma and urinary osmolality occurred. Those clinical and biological parameters remained normal thereafter.
Discussion. Based on our observation, this case of hyponatremia was suggestive of a syndrome of inappropriate ADH secretion (SIADH), with neither signs of renal or cardiac failure nor associated hypotensive or hypovolemic factors. Moreover, normality of blood volume as well as adrenal, renal, cardiac, hepatic, and thyroid functions was consistent with SIADH.
Absence of high levels of ADH does not affect our diagnosis. Actually, the ADH level is not essential for SIADH diagnosis, and cases have been reported with normal or low plasma ADH values, suggesting an increase in renal sensitivity to ADH.1 Use of the Naranjo probability scale indicated a possible relationship between hyponatremia and esomeprazole therapy in this patient.2 Spironolactone was unlikely to be associated with this adverse effect, since resolution of hyponatremia occurred after esomeprazole interruption despite continuation of spironolactone therapy (which, by increasing urinary sodium levels, can contribute to hyponatremia).
SIADH cases associated with use of PPIs have been rarely reported in the medical literature. Durst et al.3 suggested a relationship between omeprazole therapy and SIADH. The etiology of the development of SIADH in association with PPIs is yet to be established. However, an excessive loss of urinary sodium seems more probable than sole water retention.4 For the most part, this adverse drug reaction is generally encountered in elderly patients in relation with physiologic changes in water and electrolyte balance that occur as part of the aging process.5
Conclusions. The relationship between hyponatremia and esomeprazole therapy cannot be explained by cross-reactivity between PPIs because the patient had not developed hyponatremia while taking lansoprazole. Hyponatremia may rarely be associated with PPIs, but clinicians should be aware of this possible adverse reaction.
References
This article has been cited by other articles:
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  M. A. Munger New agents for managing hyponatremia in hospitalized patients Am. J. Health Syst. Pharm., February 1, 2007; 64(3): 253 - 265. [Abstract] [Full Text] [PDF]
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